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Paracaspase MALT1 deficiency protects mice from autoimmune-mediated demyelination

(2013) JOURNAL OF IMMUNOLOGY. 190(6). p.2896-2903
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Abstract
The paracaspase MALT 1 is a major player in lymphocyte activation and proliferation. MALT1 mediates Ag-induced signaling to the transcription factor NF-kappa B by functioning both as a scaffold protein and cysteine protease. We studied the role of MALT1 in the development of experimental autoimmune encephalomyelitis (EAE), an animal model of multiple sclerosis. MALT1-knockout mice did not develop any clinical symptoms of EAE. In addition, lymphocyte and macrophage infiltration into the spinal cord was absent in MALT1-knockout mice, as were demyelination and proinflammatory gene expression. Adoptive transfer experiments showed that MALT1 deficiency in splenocytes is sufficient for EAE resistance. Moreover, autoreactive T cell activation was severely impaired in MALT1-deficient T cells, suggesting the inability of MALT1-deficient effector T cells to induce demyelinating inflammation in the CNS. Finally, the MALT1 substrates A20 and CYLD were completely processed in wild-type T cells during EAE, which was partially impaired in MALT1-deficient T cells, suggesting a contribution of MALT1 proteolytic activity in T cell activation and EAE development. Together, our data indicate that MALT1 may be an interesting therapeutic target in the treatment of multiple sclerosis.
Keywords
C-REL, ABC-DLBCL, ENCEPHALOMYELITIS, MULTIPLE-SCLEROSIS, AUTOREACTIVE T-CELLS, NF-KAPPA-B, CYLD, IMMUNE, A20, ACTIVATION

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MLA
Mc Guire, Conor, et al. “Paracaspase MALT1 Deficiency Protects Mice from Autoimmune-Mediated Demyelination.” JOURNAL OF IMMUNOLOGY, vol. 190, no. 6, 2013, pp. 2896–903.
APA
Mc Guire, C., Wieghofer, P., Elton, L., Muylaert, D., Prinz, M., Beyaert, R., & van Loo, G. (2013). Paracaspase MALT1 deficiency protects mice from autoimmune-mediated demyelination. JOURNAL OF IMMUNOLOGY, 190(6), 2896–2903.
Chicago author-date
Mc Guire, Conor, Peter Wieghofer, Lynn Elton, David Muylaert, Marco Prinz, Rudi Beyaert, and Geert van Loo. 2013. “Paracaspase MALT1 Deficiency Protects Mice from Autoimmune-Mediated Demyelination.” JOURNAL OF IMMUNOLOGY 190 (6): 2896–2903.
Chicago author-date (all authors)
Mc Guire, Conor, Peter Wieghofer, Lynn Elton, David Muylaert, Marco Prinz, Rudi Beyaert, and Geert van Loo. 2013. “Paracaspase MALT1 Deficiency Protects Mice from Autoimmune-Mediated Demyelination.” JOURNAL OF IMMUNOLOGY 190 (6): 2896–2903.
Vancouver
1.
Mc Guire C, Wieghofer P, Elton L, Muylaert D, Prinz M, Beyaert R, et al. Paracaspase MALT1 deficiency protects mice from autoimmune-mediated demyelination. JOURNAL OF IMMUNOLOGY. 2013;190(6):2896–903.
IEEE
[1]
C. Mc Guire et al., “Paracaspase MALT1 deficiency protects mice from autoimmune-mediated demyelination,” JOURNAL OF IMMUNOLOGY, vol. 190, no. 6, pp. 2896–2903, 2013.
@article{3182275,
  abstract     = {The paracaspase MALT 1 is a major player in lymphocyte activation and proliferation. MALT1 mediates Ag-induced signaling to the transcription factor NF-kappa B by functioning both as a scaffold protein and cysteine protease. We studied the role of MALT1 in the development of experimental autoimmune encephalomyelitis (EAE), an animal model of multiple sclerosis. MALT1-knockout mice did not develop any clinical symptoms of EAE. In addition, lymphocyte and macrophage infiltration into the spinal cord was absent in MALT1-knockout mice, as were demyelination and proinflammatory gene expression. Adoptive transfer experiments showed that MALT1 deficiency in splenocytes is sufficient for EAE resistance. Moreover, autoreactive T cell activation was severely impaired in MALT1-deficient T cells, suggesting the inability of MALT1-deficient effector T cells to induce demyelinating inflammation in the CNS. Finally, the MALT1 substrates A20 and CYLD were completely processed in wild-type T cells during EAE, which was partially impaired in MALT1-deficient T cells, suggesting a contribution of MALT1 proteolytic activity in T cell activation and EAE development. Together, our data indicate that MALT1 may be an interesting therapeutic target in the treatment of multiple sclerosis.},
  author       = {Mc Guire, Conor and Wieghofer, Peter and Elton, Lynn and Muylaert, David and Prinz, Marco and Beyaert, Rudi and van Loo, Geert},
  issn         = {0022-1767},
  journal      = {JOURNAL OF IMMUNOLOGY},
  keywords     = {C-REL,ABC-DLBCL,ENCEPHALOMYELITIS,MULTIPLE-SCLEROSIS,AUTOREACTIVE T-CELLS,NF-KAPPA-B,CYLD,IMMUNE,A20,ACTIVATION},
  language     = {eng},
  number       = {6},
  pages        = {2896--2903},
  title        = {Paracaspase MALT1 deficiency protects mice from autoimmune-mediated demyelination},
  url          = {http://dx.doi.org/10.4049/jimmunol.1201351},
  volume       = {190},
  year         = {2013},
}

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